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Molecular and Cellular Biology, July 2001, p. 4119-4128, Vol. 21, No. 13
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.13.4119-4128.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Loss of Annexin A7 Leads to Alterations in Frequency-Induced Shortening of Isolated Murine Cardiomyocytes

Claudia Herr,1 Neil Smyth,2 Susanne Ullrich,3 Fan Yun,3 Phillip Sasse,3 Jürgen Hescheler,3 Bernd Fleischmann,3 Katrin Lasek,4 Klara Brixius,4 Robert H. G. Schwinger,4 Reinhard Fässler,5 Rolf Schröder,6 and Angelika A. Noegel1,*

Institute of Biochemistry I1 and II,2 Department of Neurophysiology,3 and Laboratory of Muscle Research and Molecular Cardiology, Clinic III of Internal Medicine,4 University of Cologne, 50931 Cologne, and Department of Neurology, University Hospital Bonn, Bonn,6 Germany, and Department of Experimental Pathology, Lund University, Lund, Sweden5

Received 21 December 2000/Returned for modification 1 February 2001/Accepted 6 April 2001

Annexin A7 has been proposed to function in the fusion of vesicles, acting as a Ca2+ channel and as Ca2+-activated GTPase, thus inducing Ca2+/GTP-dependent secretory events. To understand the function of annexin A7, we have performed targeted disruption of the Anxa7 gene in mice. Matings between heterozygous mice produced offspring showing a normal Mendelian pattern of inheritance, indicating that the loss of annexin A7 did not interfere with viability in utero. Mice lacking annexin A7 showed no obvious phenotype and were fertile. To assay for exocytosis, insulin secretion from isolated islets of Langerhans was examined. Ca2+-induced and cyclic AMP-mediated potentiation of insulin secretion was unchanged in the absence of annexin A7, suggesting that it is not directly implicated in vesicle fusion. Ca2+ regulation studied in isolated cardiomyocytes, showed that while cells from early embryos displayed intact Ca2+ homeostasis and expressed all of the components required for excitation-contraction coupling, cardiomyocytes from adult Anxa7-/- mice exhibited an altered cell shortening-frequency relationship when stimulated with high frequencies. This suggests a function for annexin A7 in electromechanical coupling, probably through Ca2+ homoeostasis.

* Corresponding author. Mailing address: Institute of Biochemistry I, Joseph-Stelzmann-Str. 52, 50931 Cologne, Germany. Phone: 49 221 478 6980. Fax: 49 221 478 6979. E-mail: noegel{at}uni-koeln.de.

Molecular and Cellular Biology, July 2001, p. 4119-4128, Vol. 21, No. 13
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.13.4119-4128.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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